SUMMARYWater deprivation was produced in pregnant sheep by withholding water for 24 h and then giving them 500 ml/d for the subsequent 3 d. All ewes bore chronically cannulated fetuses. Eleven experiments were performed in group I animals (gestation periods of 107-119 d at maximal stress) and eight experiments in group II (126-144 d of gestation). Measurements were made of maternal and fetal plasma osmolalities, fetal urine flow rate and osmolality, amniotic fluid osmolality and fetal plasma antidiuretic hormone (ADH) concentration. The experimental protocol produced a larger increment in maternal and fetal plasma osmolalities in group I than in group II (P < 0 025). For group I fetuses the relationship between plasma ADH concentration, [ADH] and plasma osmolality was log [ADH] = -4-50+0-0174 (osmol) which was significantly different from that for group II fetuses, log [ADHI = -1046+0-0373 (osmol) (P < 0-02). Thus plasma [ADH] was significantly greater, at a given plasma osmolality, in older (group II) than younger (group I) fetuses. For a given value of fetal plasma [ADH] there was a greater reduction in fetal urine free water clearance in older than younger fetuses. Water deprivation of the ewe did disturb the composition of amniotic fluid and the trend in amniotic fluid osmolality followed the trend in fetal urinary osmolality.

Fructose (FR) consumption is a major contributor to obesity and chronic inflammation but its effects have not been widely studied in pregnancy. Pregnancy is a state of systemic inflammation, and increased expression of inflammatory markers in pregnancy has been associated with pre‐eclampsia and other vascular complications; many of these markers may arise from adipose tissue. The study investigated the effect of FR consumption during gestation and its effect on obesity and inflammatory markers (leptin, mass and obesity‐associated (FTO) gene and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐kB) gene) Female rats received either 10% FR solution (n=18) or tap water (CNTL) (n=17) during gestation. Pregnancies were terminated at gestation day 20; adipose tissue was frozen and total RNA extracted for real time PCR analysis. mRNA abundance was performed for the genes encoding leptin, FTO gene and NF‐kB with housekeeping gene 18s. mRNA expression of FTO (FR:1.75( 0.3; CNTL: 1( 0.1; p<0.05), NF‐?B (FR:1.67( 0.2; CNTL: 1( 0.2; p<0.05) and leptin (FR:2.1( 0.5; CNTL: 1( 0.1; p<0.05) were all upregulated with the FR group. Maternal weight exhibited no difference between the FR and CNTL groups even though markers of obesity and inflammation showed enhanced expression. Further research on inflammatory markers is required to examine the state of systemic inflammation present. Funded by NSERC Canada

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